Diabetic nephropathy is a progressive kidney disease caused by vascular damage to the glomerular capillaries and arterioles as a consequence of long-standing hyperglycemia. Classically, this is characterized by progressive proteinuria followed by renal insufficiency. It can eventually lead to end-stage renal disease.

Patients with type 1 diabetes mellitus generally develop diabetic kidney disease within 10 years after diagnosis. There is more variability with diagnosis in patients with type 2 diabetes, as some people may never be affected and others lose renal function very quickly after diagnosis. Diabetic nephropathy is more common and more severe in African American and Latino populations. Aging, obesity, smoking, and poorly controlled hypertension are also risk factors for this condition.

Many physiologic factors are involved in the pathogenesis of this disease. Generally, chronic elevated serum glucose causes nonenzymatic glycosylation of the vasculature in the kidneys. Cytokines and other inflammatory markers have also been implicated in activating multiple pathways that contribute to glomerular damage over time. These mechanisms lead to hyaline arteriosclerosis, endothelial damage, and podocyte loss, which increase the glomerular filtration pressure and contribute to loss of proteins in the urine. This is a secondary cause of nephrotic syndrome.